Catalpol downregulates vascular endothelial‑cadherin expression and induces vascular hyperpermeability.

Abstract

Catalpol, an iridiod glucoside isolated from Rehmannia glutinosa, has been reported to possess anti‑inflammatory properties. However, the molecular mechanisms underlying this effect have not been fully elucidated. This study aimed to investigate the effects of catalpol on vascular permeability. Using Transwell permeability assays and measurements of trans‑endothelial electrical resistance (TEER), it was demonstrated that 1 mM catalpol induces a significant increase in the permeability of the monolayers of human umbilical vein endothelial cells (HUVECs). Western blotting and immunofluorescence demonstrated that catalpol inhibits the expression of vascular endothelial (VE)‑cadherin, the key component of adherens junctions, but not occludin, the major constituent of tight junctions. In addition, catalpol inhibits the ETS transcription factor ERG, a positive regulator of VE‑cadherin. Knockdown of ERG expression compromised the catalpol‑induced reduction of TEER in HUVECs. The present study revealed a novel effect of catalpol on vascular permeability and gave insight into the multifaceted roles of catalpol in inflammation.

• Authors: Caiqing Zhang, Qingfa Liu, Fengyun Dong, Liqun Li, Juan Du, Qi Xie, Hesheng Hu, Suhua Yan, Xia Zhou, Changsheng Li, Corrinne G Lobe, Ju Liu
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 13 Issue 1 Pg. 373-8 (Jan 2016) ISSN: 1791-3004 [Electronic] Greece
• PMID: 26549479 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antigens, CD
• Cadherins
• ERG protein, human
• Iridoid Glucosides
• Occludin
• Trans-Activators
• Transcriptional Regulator ERG
• cadherin 5
• catalpol

Topics

• Antigens, CD (metabolism)
• Cadherins (metabolism)
• Capillary Permeability (drug effects)
• Dose-Response Relationship, Drug
• Down-Regulation (drug effects)
• Endothelium, Vascular (drug effects, metabolism)
• Human Umbilical Vein Endothelial Cells (drug effects, metabolism)
• Humans
• Iridoid Glucosides (pharmacology)
• Occludin (metabolism)
• Protein Transport (drug effects)
• Trans-Activators (metabolism)
• Transcriptional Regulator ERG